Endothelin Type B Receptor–Induced Sustained Ca2+ Influx Involves Gq/11/Phospholipase C–Independent, p38 Mitogen-Activated Protein Kinase–Dependent Activation of Na+/H+ Exchanger

Tsunaki Higa; Takahiro Horinouchi; Hiroyuki Aoyagi; Hiroshi Asano; Tadashi Nishiya; Arata Nishimoto; Ikunobu Muramatsu; Soichi Miwa

doi:10.1254/jphs.10102SC

Short Communications

Endothelin Type B Receptor–Induced Sustained Ca²⁺ Influx Involves G_q/11/Phospholipase C–Independent, p38 Mitogen-Activated Protein Kinase–Dependent Activation of Na⁺/H⁺ Exchanger

Tsunaki Higa, Takahiro Horinouchi, Hiroyuki Aoyagi, Hiroshi Asano, Tadashi Nishiya, Arata Nishimoto, Ikunobu Muramatsu, Soichi Miwa

著者情報

キーワード: endothelin type B receptor, Na⁺/H⁺ exchanger, p38 mitogen-activated protein kinase

ジャーナルフリー

2010 年 113 巻 3 号 p. 276-280

DOI https://doi.org/10.1254/jphs.10102SC

View "Advance Publication" version (June 29, 2010).

詳細

抄録

The mechanism for sustained Ca²⁺ influx activated by G protein–coupled receptors was examined. In Chinese hamster ovary cells expressing recombinant human endothelin type B receptor (ET_BR) and endogenous P2Y receptor (P2Y-R), endothelin-1 elicited a sustained Ca²⁺ influx depending on G_q/11protein, phospholipase C (PLC), Na⁺/H⁺ exchanger (NHE), and p38 mitogen-activated protein kinase (p38MAPK), whereas P2Y-R–induced sustained Ca²⁺ influx was negligible. Functional studies showed that NHE activation by ET_BR was mediated via p38MAPK but not G_q/11/PLC, while that by P2Y-R involves only G_q/11/PLC/p38MAPK. These results suggest that G_q/11/PLC-independent NHE activation via p38MAPK plays an important role in ET_BR- mediated sustained Ca²⁺ influx.

責任著者(Corresponding author)

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